Journal: Brain Pathology

Article Title: Relevance of host tau in tau seeding and spreading in tauopathies

doi: 10.1111/bpa.12778

Figure Lengend Snippet: Characteristics of the antibodies used.

Article Snippet: NeuN , Monoclonal , 1:100 , Merck‐Millipore , Billerica, MA, USA.

Techniques: Ubiquitin Proteomics

Journal: Experimental Biology and Medicine

Article Title: Annona atemoya leaf extract ameliorates cognitive impairment in amyloid-β injected Alzheimer’s disease-like mouse model

doi: 10.1177/1535370219886269

Figure Lengend Snippet: Effects of AAL extract on memory impairment in an Aβ-induced AD-like mouse model. (a) Time schedule of the animal experiments. (b) Male ICR mice were assigned to five groups (n = 7/group). Aβ aggregates (50 pmol per 10% DMSO in PBS) were injected into the intracerebroventricular region. Vehicle (saline), AAL (50 or 100 mg/kg), or morin (10 mg/kg) was orally administered for 23 days after adaptation for one week. (b) For the passive avoidance test, mice were trained on a one-trial step-through passive avoidance task on day 14 after Aβ injection (retention trial). The testing trial was given two days after the training trial (acquisition trial). The latency time was recorded at the retention and acquisition trials. (c) Y-maze was performed on day 18 after Aβ injection. Spontaneous alternation behavior was measured during an 8-min session. The data are presented as means ± SEM. ##P < 0.01 vs. normal group. *P < 0.05, and ***P < 0.001 vs. Aβ control group. Morin was used as a positive control for inhibitor of Aβ aggregation. (d) Expression of NeuN and BDNF in hippocampus was determined by immunohistochemistry (magnification ×200). (e) Quantification of the BDNF positive stained cell density within the hippocampus (proportion of BDNF positive staining over the hippocampus area) was compared between experimental groups (section from n = 3 brains were analyzed per group). (f) The number of neurons in different areas of the brain was estimated by automated cell counting (particle analysis) using the Image J software. NC: normal control, AAL: Annona atemoya leaf. (A color version of this figure is available in the online journal.)

Article Snippet: For immunohistochemical assays, briefly rinsed brain sections were incubated with rabbit anti-neuronal nuclei (NeuN) (Merck Millipore, Darmstadt, Germany) at 4°C for overnight with normal goat serum and 0.3% Triton X-100.

Techniques: Injection, Saline, Control, Positive Control, Expressing, Immunohistochemistry, Staining, Cell Counting, Particle Size Analysis, Software

Journal: Journal of Neuroinflammation

Article Title: Zika virus infection of mature neurons from immunocompetent mice generates a disease-associated microglia and a tauopathy-like phenotype in link with a delayed interferon beta response

doi: 10.1186/s12974-022-02668-8

Figure Lengend Snippet: ZIKV-infection induces the activation of microglia and of IFNs-I and pro-inflammatory responses in the brain of immunocompetent CC071 mice, in the absence of microglia infection. CC001 and CC071 mice (5–6 week-old) were necropsied at day 6 following IC inoculation of either PBS or 10 5 FFU of ZIKV. a – e As compared to non-susceptible CC001 mice, ZIKV infection of susceptible CC071 mice induced a significantly higher expression of mRNAs coding a for IFNB and ISGs and for factors associated with the b the pro-inflammatory response and c the complement cascade without significantly affecting genes associated with d the anti-inflammatory response and e the homeostatic “off” state of microglia as determined by RT-qPCR analysis of total brain extracts with respect to Hrpt1 used as reference gene. Symbols represent individual mice. Data from n = 5 CC001 and CC071 mice respectively are means without s.d. with significance assessed by two-way ANOVA Tukey’s multiple comparisons test. P -value < 0.0001 (****), < 0.001 (***), < 0.01 (**), < 0.05 (*) and ns not significant; P -values comprised between 0.05 and 0.1 (considered as near significant) are indicated. f , g ZIKV induced microglia activation in CC071 mice brains while only infecting neurons as determined by immunofluorescence and confocal microscopy with neurons labeled with anti-NeuN (green), microglial cells with anti-Iba1 antibody (red), ZIKV-infected cells with anti-NS2B antibody (red or green) and DNA labeled with DAPI (blue). Single confocal sections (z projection) and the corresponding merge images are shown. Scale bars in f 10 µm and g 20 µm

Article Snippet: Primary antibodies used for immunofluorescence and/or Western blot (WB) were: anti-GSK-3α/β (sc-7291), anti-pGSK-3α/β (sc-81496) and anti-βActin (sc-47778) from SantaCruz; anti-MAP2 (188002) from Synaptic Systems; anti-beta tubulin III, TUJ1 (MAB 1637) from Millipore; anti-pTau antibodies: AT8 (MN1020) and AT100 (MN1060) from ThermoFisher and AD2 from the laboratory Alzheimer & Tauopathies (LilNCog, Lille, France) [ ]; anti-NeuN (GTX16208) and anti-ZIKV protein NS2B (GTX133308) from GeneTex; anti-Iba1 (5076) from Abcam and (019-19741) from Wako.

Techniques: Infection, Activation Assay, Expressing, Quantitative RT-PCR, Immunofluorescence, Confocal Microscopy, Labeling